scholarly journals Chlamydia pneumoniaeAlters Mildly Oxidized Low‐Density Lipoprotein–Induced Cell Death in Human Endothelial Cells, Leading to Necrosis Rather Than Apoptosis

2006 ◽  
Vol 193 (1) ◽  
pp. 136-145 ◽  
Author(s):  
Dani Nazzal ◽  
Anne‐Valérie Cantéro ◽  
Nicole Therville ◽  
Bruno Ségui ◽  
Anne Nègre‐Salvayre ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Human Endothelial Cells

scholarly journals Oxidized low-density lipoprotein induces calpain-dependent cell death and ubiquitination of caspase 3 in HMEC-1 endothelial cells

2003 ◽  
Vol 374 (2) ◽  
pp. 403-411 ◽  
Author(s):  
M. Isabella PÖRN-ARES ◽  
Takaomi C. SAIDO ◽  
Tommy ANDERSSON ◽  
Mikko P. S. ARES
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Caspase 3 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Calpain Inhibitor ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Nucleosomal Dna ◽  
General Caspase Inhibitor

Oxidized low-density lipoprotein (oxLDL) is known to induce apoptosis in endothelial cells, and this is believed to contribute to the progression of atherosclerosis. In the present study we made the novel observation that oxLDL-induced death of HMEC-1 cells is accompanied by activation of calpain. The μ-calpain inhibitor PD 151746 decreased oxLDL-induced cytotoxicity, whereas the general caspase inhibitor BAF (t-butoxycarbonyl-Asp-methoxyfluoromethylketone) had no effect. Also, oxLDL provoked calpain-dependent proteolysis of cytoskeletal α-fodrin in the HMEC-1 cells. Our observation of an autoproteolytic cleavage of the 80 kDa subunit of μ-calpain provided further evidence for an oxLDL-induced stimulation of calpain activity. The Bcl-2 protein Bid was also cleaved during oxLDL-elicited cell death, and this was prevented by calpain inhibitors, but not by inhibitors of cathepsin B and caspases. Treating the HMEC-1 cells with oxLDL did not result in detectable activation of procaspase 3 or cleavage of PARP [poly(ADP-ribose) polymerase], but it did cause polyubiquitination of caspase 3, indicating inactivation and possible degradation of this protease. Despite the lack of caspase 3 activation, oxLDL treatment led to the formation of nucleosomal DNA fragments characteristic of apoptosis. These novel results show that oxLDL initiates a calpain-mediated death-signalling pathway in endothelial cells.

scholarly journals Induction of NAD(P)H Oxidase by Oxidized Low-Density Lipoprotein in Human Endothelial Cells

Circulation ◽  
2001 ◽  
Vol 104 (15) ◽  
pp. 1767-1772 ◽  
Author(s):  
Uwe Rueckschloss ◽  
Jan Galle ◽  
Juergen Holtz ◽  
Hans-Reinhard Zerkowski ◽  
Henning Morawietz
Keyword(s):  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Human Endothelial Cells
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